{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["van Dijk AD"],"funding":["NCI","NIH COG","Junior Scientific Masterclass (Groningen, The Netherlands)","NCI NIH HHS"],"pagination":["1448"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11048007"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(8)"],"pubmed_abstract":["The addition of the proteasome inhibitor bortezomib to standard chemotherapy did not improve survival in pediatric acute myeloid leukemia (AML) when all patients were analyzed as a group in the Children's Oncology Group phase 3 trial AAML1031 (NCT01371981). Proteasome inhibition influences the chromatin landscape and proteostasis, and we hypothesized that baseline proteomic analysis of histone- and chromatin-modifying enzymes (HMEs) would identify AML subgroups that benefitted from bortezomib addition. A proteomic profile of 483 patients treated with AAML1031 chemotherapy was generated using a reverse-phase protein array. A relatively high expression of 16 HME was associated with lower EFS and higher 3-year relapse risk after AML standard treatment compared to low expressions (52% vs. 29%,"],"journal":["Cancers"],"pubmed_title":["Chromatin Profiles Are Prognostic of Clinical Response to Bortezomib-Containing Chemotherapy in Pediatric Acute Myeloid Leukemia: Results from the COG AAML1031 Trial."],"pmcid":["PMC11048007"],"funding_grant_id":["U10 CA180886","U10 CA98543","R01-CA164024","U24 CA196173","U10 CA180899","U10 CA98413"],"pubmed_authors":["van Dijk AD","Leonti AR","Meshinchi S","Hubner SE","de Bont ESJM","Go RL","Gerbing RB","Qiu Y","Kornblau SM","Gamis AS","Horton TM","Aplenc R","Hoff FW","Alonzo TA","Ruvolo VR","Kolb EA"],"additional_accession":[]},"is_claimable":false,"name":"Chromatin Profiles Are Prognostic of Clinical Response to Bortezomib-Containing Chemotherapy in Pediatric Acute Myeloid Leukemia: Results from the COG AAML1031 Trial.","description":"The addition of the proteasome inhibitor bortezomib to standard chemotherapy did not improve survival in pediatric acute myeloid leukemia (AML) when all patients were analyzed as a group in the Children's Oncology Group phase 3 trial AAML1031 (NCT01371981). Proteasome inhibition influences the chromatin landscape and proteostasis, and we hypothesized that baseline proteomic analysis of histone- and chromatin-modifying enzymes (HMEs) would identify AML subgroups that benefitted from bortezomib addition. A proteomic profile of 483 patients treated with AAML1031 chemotherapy was generated using a reverse-phase protein array. A relatively high expression of 16 HME was associated with lower EFS and higher 3-year relapse risk after AML standard treatment compared to low expressions (52% vs. 29%,","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-04-08T19:52:15.017Z","creation":"2026-04-08T14:32:43.348Z"},"accession":"S-EPMC11048007","cross_references":{"pubmed":["38672531"],"doi":["10.3390/cancers16081448"]}}